Salvianolic Acid B (Sal B) Protects Retinal Pigment Epithelial Cells from Oxidative Stress-Induced Cell Death by Activating Glutaredoxin 1 (Grx1).
Identifieur interne : 000418 ( Main/Exploration ); précédent : 000417; suivant : 000419Salvianolic Acid B (Sal B) Protects Retinal Pigment Epithelial Cells from Oxidative Stress-Induced Cell Death by Activating Glutaredoxin 1 (Grx1).
Auteurs : Xiaobin Liu [États-Unis] ; Christy Xavier [États-Unis] ; Jamieson Jann [États-Unis] ; Hongli Wu [États-Unis]Source :
- International journal of molecular sciences [ 1422-0067 ] ; 2016.
Descripteurs français
- KwdFr :
- Activation enzymatique (effets des médicaments et des substances chimiques), Antioxydants (pharmacologie), Benzofuranes (pharmacologie), Cellules épithéliales (cytologie), Cellules épithéliales (effets des médicaments et des substances chimiques), Cellules épithéliales (métabolisme), Culture de cellules primaires (MeSH), Disulfures (métabolisme), Facteur-2 apparenté à NF-E2 (agonistes), Facteur-2 apparenté à NF-E2 (génétique), Facteur-2 apparenté à NF-E2 (métabolisme), Facteurs temps (MeSH), Foetus (MeSH), Glutarédoxines (antagonistes et inhibiteurs), Glutarédoxines (génétique), Glutarédoxines (métabolisme), Glutathion (métabolisme), Humains (MeSH), Médicaments issus de plantes chinoises (pharmacologie), Oxydoréduction (MeSH), Peroxyde d'hydrogène (antagonistes et inhibiteurs), Peroxyde d'hydrogène (pharmacologie), Petit ARN interférent (génétique), Petit ARN interférent (métabolisme), Relation dose-effet des médicaments (MeSH), Régulation de l'expression des gènes (MeSH), Stress oxydatif (MeSH), Transduction du signal (MeSH), Épithélium pigmentaire de la rétine (cytologie), Épithélium pigmentaire de la rétine (effets des médicaments et des substances chimiques), Épithélium pigmentaire de la rétine (métabolisme).
- MESH :
- agonistes : Facteur-2 apparenté à NF-E2.
- antagonistes et inhibiteurs : Glutarédoxines, Peroxyde d'hydrogène.
- cytologie : Cellules épithéliales, Épithélium pigmentaire de la rétine.
- effets des médicaments et des substances chimiques : Activation enzymatique, Cellules épithéliales, Épithélium pigmentaire de la rétine.
- génétique : Facteur-2 apparenté à NF-E2, Glutarédoxines, Petit ARN interférent.
- métabolisme : Cellules épithéliales, Disulfures, Facteur-2 apparenté à NF-E2, Glutarédoxines, Glutathion, Petit ARN interférent, Épithélium pigmentaire de la rétine.
- pharmacologie : Antioxydants, Benzofuranes, Médicaments issus de plantes chinoises, Peroxyde d'hydrogène.
- Culture de cellules primaires, Facteurs temps, Foetus, Humains, Oxydoréduction, Relation dose-effet des médicaments, Régulation de l'expression des gènes, Stress oxydatif, Transduction du signal.
English descriptors
- KwdEn :
- Antioxidants (pharmacology), Benzofurans (pharmacology), Disulfides (metabolism), Dose-Response Relationship, Drug (MeSH), Drugs, Chinese Herbal (pharmacology), Enzyme Activation (drug effects), Epithelial Cells (cytology), Epithelial Cells (drug effects), Epithelial Cells (metabolism), Fetus (MeSH), Gene Expression Regulation (MeSH), Glutaredoxins (antagonists & inhibitors), Glutaredoxins (genetics), Glutaredoxins (metabolism), Glutathione (metabolism), Humans (MeSH), Hydrogen Peroxide (antagonists & inhibitors), Hydrogen Peroxide (pharmacology), NF-E2-Related Factor 2 (agonists), NF-E2-Related Factor 2 (genetics), NF-E2-Related Factor 2 (metabolism), Oxidation-Reduction (MeSH), Oxidative Stress (MeSH), Primary Cell Culture (MeSH), RNA, Small Interfering (genetics), RNA, Small Interfering (metabolism), Retinal Pigment Epithelium (cytology), Retinal Pigment Epithelium (drug effects), Retinal Pigment Epithelium (metabolism), Signal Transduction (MeSH), Time Factors (MeSH).
- MESH :
- chemical , agonists : NF-E2-Related Factor 2.
- chemical , antagonists & inhibitors : Glutaredoxins, Hydrogen Peroxide.
- chemical , genetics : Glutaredoxins, NF-E2-Related Factor 2, RNA, Small Interfering.
- chemical , metabolism : Disulfides, Glutaredoxins, Glutathione, NF-E2-Related Factor 2, RNA, Small Interfering.
- chemical , pharmacology : Antioxidants, Benzofurans, Drugs, Chinese Herbal, Hydrogen Peroxide.
- cytology : Epithelial Cells, Retinal Pigment Epithelium.
- drug effects : Enzyme Activation, Epithelial Cells, Retinal Pigment Epithelium.
- metabolism : Epithelial Cells, Retinal Pigment Epithelium.
- Dose-Response Relationship, Drug, Fetus, Gene Expression Regulation, Humans, Oxidation-Reduction, Oxidative Stress, Primary Cell Culture, Signal Transduction, Time Factors.
Abstract
Protein glutathionylation, defined as the formation of protein mixed disulfides (PSSG) between cysteine residues and glutathione (GSH), can lead to cell death. Glutaredoxin 1 (Grx1) is a thiol repair enzyme which catalyzes the reduction of PSSG. Therefore, Grx1 exerts strong anti-apoptotic effects by improving the redox state, especially in times of oxidative stress. However, there is currently no compound that is identified as a Grx1 activator. In this study, we identified and characterized Salvianolic acid B (Sal B), a natural compound, as a Grx1 inducer, which potently protected retinal pigment epithelial (RPE) cells from oxidative injury. Our results showed that treatment with Sal B protected primary human RPE cells from H₂O₂-induced cell damage. Interestingly, we found Sal B pretreatment upregulated Grx1 expression in RPE cells in a time- and dose-dependent manner. Furthermore, NF-E2-related factor 2 (Nrf2), the key transcription factor that regulates the expression of Grx1, was activated in Sal B treated RPE cells. Further investigation showed that knockdown of Grx1 by small interfering RNA (siRNA) significantly reduced the protective effects of Sal B. We conclude that Sal B protects RPE cells against H₂O₂-induced cell injury through Grx1 induction by activating Nrf2 pathway, thus preventing lethal accumulation of PSSG and reversing oxidative damage.
DOI: 10.3390/ijms17111835
PubMed: 27827892
PubMed Central: PMC5133836
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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<term>Benzofurans (pharmacology)</term>
<term>Disulfides (metabolism)</term>
<term>Dose-Response Relationship, Drug (MeSH)</term>
<term>Drugs, Chinese Herbal (pharmacology)</term>
<term>Enzyme Activation (drug effects)</term>
<term>Epithelial Cells (cytology)</term>
<term>Epithelial Cells (drug effects)</term>
<term>Epithelial Cells (metabolism)</term>
<term>Fetus (MeSH)</term>
<term>Gene Expression Regulation (MeSH)</term>
<term>Glutaredoxins (antagonists & inhibitors)</term>
<term>Glutaredoxins (genetics)</term>
<term>Glutaredoxins (metabolism)</term>
<term>Glutathione (metabolism)</term>
<term>Humans (MeSH)</term>
<term>Hydrogen Peroxide (antagonists & inhibitors)</term>
<term>Hydrogen Peroxide (pharmacology)</term>
<term>NF-E2-Related Factor 2 (agonists)</term>
<term>NF-E2-Related Factor 2 (genetics)</term>
<term>NF-E2-Related Factor 2 (metabolism)</term>
<term>Oxidation-Reduction (MeSH)</term>
<term>Oxidative Stress (MeSH)</term>
<term>Primary Cell Culture (MeSH)</term>
<term>RNA, Small Interfering (genetics)</term>
<term>RNA, Small Interfering (metabolism)</term>
<term>Retinal Pigment Epithelium (cytology)</term>
<term>Retinal Pigment Epithelium (drug effects)</term>
<term>Retinal Pigment Epithelium (metabolism)</term>
<term>Signal Transduction (MeSH)</term>
<term>Time Factors (MeSH)</term>
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<term>Antioxydants (pharmacologie)</term>
<term>Benzofuranes (pharmacologie)</term>
<term>Cellules épithéliales (cytologie)</term>
<term>Cellules épithéliales (effets des médicaments et des substances chimiques)</term>
<term>Cellules épithéliales (métabolisme)</term>
<term>Culture de cellules primaires (MeSH)</term>
<term>Disulfures (métabolisme)</term>
<term>Facteur-2 apparenté à NF-E2 (agonistes)</term>
<term>Facteur-2 apparenté à NF-E2 (génétique)</term>
<term>Facteur-2 apparenté à NF-E2 (métabolisme)</term>
<term>Facteurs temps (MeSH)</term>
<term>Foetus (MeSH)</term>
<term>Glutarédoxines (antagonistes et inhibiteurs)</term>
<term>Glutarédoxines (génétique)</term>
<term>Glutarédoxines (métabolisme)</term>
<term>Glutathion (métabolisme)</term>
<term>Humains (MeSH)</term>
<term>Médicaments issus de plantes chinoises (pharmacologie)</term>
<term>Oxydoréduction (MeSH)</term>
<term>Peroxyde d'hydrogène (antagonistes et inhibiteurs)</term>
<term>Peroxyde d'hydrogène (pharmacologie)</term>
<term>Petit ARN interférent (génétique)</term>
<term>Petit ARN interférent (métabolisme)</term>
<term>Relation dose-effet des médicaments (MeSH)</term>
<term>Régulation de l'expression des gènes (MeSH)</term>
<term>Stress oxydatif (MeSH)</term>
<term>Transduction du signal (MeSH)</term>
<term>Épithélium pigmentaire de la rétine (cytologie)</term>
<term>Épithélium pigmentaire de la rétine (effets des médicaments et des substances chimiques)</term>
<term>Épithélium pigmentaire de la rétine (métabolisme)</term>
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<keywords scheme="MESH" type="chemical" qualifier="agonists" xml:lang="en"><term>NF-E2-Related Factor 2</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Glutaredoxins</term>
<term>Hydrogen Peroxide</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Glutaredoxins</term>
<term>NF-E2-Related Factor 2</term>
<term>RNA, Small Interfering</term>
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<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Disulfides</term>
<term>Glutaredoxins</term>
<term>Glutathione</term>
<term>NF-E2-Related Factor 2</term>
<term>RNA, Small Interfering</term>
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<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antioxidants</term>
<term>Benzofurans</term>
<term>Drugs, Chinese Herbal</term>
<term>Hydrogen Peroxide</term>
</keywords>
<keywords scheme="MESH" qualifier="agonistes" xml:lang="fr"><term>Facteur-2 apparenté à NF-E2</term>
</keywords>
<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Glutarédoxines</term>
<term>Peroxyde d'hydrogène</term>
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<keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Cellules épithéliales</term>
<term>Épithélium pigmentaire de la rétine</term>
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<keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Epithelial Cells</term>
<term>Retinal Pigment Epithelium</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Enzyme Activation</term>
<term>Epithelial Cells</term>
<term>Retinal Pigment Epithelium</term>
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<term>Cellules épithéliales</term>
<term>Épithélium pigmentaire de la rétine</term>
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<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Facteur-2 apparenté à NF-E2</term>
<term>Glutarédoxines</term>
<term>Petit ARN interférent</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Epithelial Cells</term>
<term>Retinal Pigment Epithelium</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cellules épithéliales</term>
<term>Disulfures</term>
<term>Facteur-2 apparenté à NF-E2</term>
<term>Glutarédoxines</term>
<term>Glutathion</term>
<term>Petit ARN interférent</term>
<term>Épithélium pigmentaire de la rétine</term>
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<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antioxydants</term>
<term>Benzofuranes</term>
<term>Médicaments issus de plantes chinoises</term>
<term>Peroxyde d'hydrogène</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Dose-Response Relationship, Drug</term>
<term>Fetus</term>
<term>Gene Expression Regulation</term>
<term>Humans</term>
<term>Oxidation-Reduction</term>
<term>Oxidative Stress</term>
<term>Primary Cell Culture</term>
<term>Signal Transduction</term>
<term>Time Factors</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Culture de cellules primaires</term>
<term>Facteurs temps</term>
<term>Foetus</term>
<term>Humains</term>
<term>Oxydoréduction</term>
<term>Relation dose-effet des médicaments</term>
<term>Régulation de l'expression des gènes</term>
<term>Stress oxydatif</term>
<term>Transduction du signal</term>
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<front><div type="abstract" xml:lang="en">Protein glutathionylation, defined as the formation of protein mixed disulfides (PSSG) between cysteine residues and glutathione (GSH), can lead to cell death. Glutaredoxin 1 (Grx1) is a thiol repair enzyme which catalyzes the reduction of PSSG. Therefore, Grx1 exerts strong anti-apoptotic effects by improving the redox state, especially in times of oxidative stress. However, there is currently no compound that is identified as a Grx1 activator. In this study, we identified and characterized Salvianolic acid B (Sal B), a natural compound, as a Grx1 inducer, which potently protected retinal pigment epithelial (RPE) cells from oxidative injury. Our results showed that treatment with Sal B protected primary human RPE cells from H₂O₂-induced cell damage. Interestingly, we found Sal B pretreatment upregulated Grx1 expression in RPE cells in a time- and dose-dependent manner. Furthermore, NF-E2-related factor 2 (Nrf2), the key transcription factor that regulates the expression of Grx1, was activated in Sal B treated RPE cells. Further investigation showed that knockdown of <i>Grx1</i>
by small interfering RNA (siRNA) significantly reduced the protective effects of Sal B. We conclude that Sal B protects RPE cells against H₂O₂-induced cell injury through Grx1 induction by activating Nrf2 pathway, thus preventing lethal accumulation of PSSG and reversing oxidative damage.</div>
</front>
</TEI>
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<DateCompleted><Year>2017</Year>
<Month>04</Month>
<Day>12</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>11</Month>
<Day>13</Day>
</DateRevised>
<Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1422-0067</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>17</Volume>
<Issue>11</Issue>
<PubDate><Year>2016</Year>
<Month>Nov</Month>
<Day>03</Day>
</PubDate>
</JournalIssue>
<Title>International journal of molecular sciences</Title>
<ISOAbbreviation>Int J Mol Sci</ISOAbbreviation>
</Journal>
<ArticleTitle>Salvianolic Acid B (Sal B) Protects Retinal Pigment Epithelial Cells from Oxidative Stress-Induced Cell Death by Activating Glutaredoxin 1 (Grx1).</ArticleTitle>
<ELocationID EIdType="pii" ValidYN="Y">E1835</ELocationID>
<Abstract><AbstractText>Protein glutathionylation, defined as the formation of protein mixed disulfides (PSSG) between cysteine residues and glutathione (GSH), can lead to cell death. Glutaredoxin 1 (Grx1) is a thiol repair enzyme which catalyzes the reduction of PSSG. Therefore, Grx1 exerts strong anti-apoptotic effects by improving the redox state, especially in times of oxidative stress. However, there is currently no compound that is identified as a Grx1 activator. In this study, we identified and characterized Salvianolic acid B (Sal B), a natural compound, as a Grx1 inducer, which potently protected retinal pigment epithelial (RPE) cells from oxidative injury. Our results showed that treatment with Sal B protected primary human RPE cells from H₂O₂-induced cell damage. Interestingly, we found Sal B pretreatment upregulated Grx1 expression in RPE cells in a time- and dose-dependent manner. Furthermore, NF-E2-related factor 2 (Nrf2), the key transcription factor that regulates the expression of Grx1, was activated in Sal B treated RPE cells. Further investigation showed that knockdown of <i>Grx1</i>
by small interfering RNA (siRNA) significantly reduced the protective effects of Sal B. We conclude that Sal B protects RPE cells against H₂O₂-induced cell injury through Grx1 induction by activating Nrf2 pathway, thus preventing lethal accumulation of PSSG and reversing oxidative damage.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Liu</LastName>
<ForeName>Xiaobin</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>Pharmaceutical Sciences, University of North Texas System College of Pharmacy, University of North Texas Health Science Center, Fort Worth, TX 76107, USA. xiaobin.liu@unthsc.edu.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Xavier</LastName>
<ForeName>Christy</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Pharmaceutical Sciences, University of North Texas System College of Pharmacy, University of North Texas Health Science Center, Fort Worth, TX 76107, USA. Christy.Xavier@unthsc.edu.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Jann</LastName>
<ForeName>Jamieson</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Pharmaceutical Sciences, University of North Texas System College of Pharmacy, University of North Texas Health Science Center, Fort Worth, TX 76107, USA. jjann@uga.edu.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wu</LastName>
<ForeName>Hongli</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>Pharmaceutical Sciences, University of North Texas System College of Pharmacy, University of North Texas Health Science Center, Fort Worth, TX 76107, USA. hongli.wu@unthsc.edu.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>North Texas Eye Research Institute, University of North Texas Health Science Center, Fort Worth, TX 76107, USA. hongli.wu@unthsc.edu.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2016</Year>
<Month>11</Month>
<Day>03</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>Switzerland</Country>
<MedlineTA>Int J Mol Sci</MedlineTA>
<NlmUniqueID>101092791</NlmUniqueID>
<ISSNLinking>1422-0067</ISSNLinking>
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<NameOfSubstance UI="D001572">Benzofurans</NameOfSubstance>
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<NameOfSubstance UI="C516005">GLRX protein, human</NameOfSubstance>
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<NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance>
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<NameOfSubstance UI="D051267">NF-E2-Related Factor 2</NameOfSubstance>
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<NameOfSubstance UI="C495635">NFE2L2 protein, human</NameOfSubstance>
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<Chemical><RegistryNumber>0</RegistryNumber>
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<NameOfSubstance UI="D006861">Hydrogen Peroxide</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>C1GQ844199</RegistryNumber>
<NameOfSubstance UI="C076944">salvianolic acid B</NameOfSubstance>
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<Chemical><RegistryNumber>GAN16C9B8O</RegistryNumber>
<NameOfSubstance UI="D005978">Glutathione</NameOfSubstance>
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<MeshHeadingList><MeshHeading><DescriptorName UI="D000975" MajorTopicYN="N">Antioxidants</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
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<MeshHeading><DescriptorName UI="D001572" MajorTopicYN="N">Benzofurans</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
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<MeshHeading><DescriptorName UI="D004220" MajorTopicYN="N">Disulfides</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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<MeshHeading><DescriptorName UI="D004305" MajorTopicYN="N">Dose-Response Relationship, Drug</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004365" MajorTopicYN="N">Drugs, Chinese Herbal</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004789" MajorTopicYN="N">Enzyme Activation</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004847" MajorTopicYN="N">Epithelial Cells</DescriptorName>
<QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005333" MajorTopicYN="N">Fetus</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005786" MajorTopicYN="N">Gene Expression Regulation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName>
<QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005978" MajorTopicYN="N">Glutathione</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006861" MajorTopicYN="N">Hydrogen Peroxide</DescriptorName>
<QualifierName UI="Q000037" MajorTopicYN="Y">antagonists & inhibitors</QualifierName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051267" MajorTopicYN="N">NF-E2-Related Factor 2</DescriptorName>
<QualifierName UI="Q000819" MajorTopicYN="N">agonists</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D010084" MajorTopicYN="N">Oxidation-Reduction</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018384" MajorTopicYN="N">Oxidative Stress</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D061251" MajorTopicYN="N">Primary Cell Culture</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D034741" MajorTopicYN="N">RNA, Small Interfering</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D055213" MajorTopicYN="N">Retinal Pigment Epithelium</DescriptorName>
<QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D013997" MajorTopicYN="N">Time Factors</DescriptorName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">glutaredoxin 1</Keyword>
<Keyword MajorTopicYN="Y">oxidative stress</Keyword>
<Keyword MajorTopicYN="Y">protein glutathionylation</Keyword>
<Keyword MajorTopicYN="Y">retinal pigment epithelial cells</Keyword>
<Keyword MajorTopicYN="Y">salvianolic acid B</Keyword>
</KeywordList>
<CoiStatement>The authors declare no conflict of interest.</CoiStatement>
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<Month>10</Month>
<Day>08</Day>
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<Month>10</Month>
<Day>31</Day>
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<Day>13</Day>
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<affiliations><list><country><li>États-Unis</li>
</country>
<region><li>Texas</li>
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<tree><country name="États-Unis"><region name="Texas"><name sortKey="Liu, Xiaobin" sort="Liu, Xiaobin" uniqKey="Liu X" first="Xiaobin" last="Liu">Xiaobin Liu</name>
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<name sortKey="Jann, Jamieson" sort="Jann, Jamieson" uniqKey="Jann J" first="Jamieson" last="Jann">Jamieson Jann</name>
<name sortKey="Wu, Hongli" sort="Wu, Hongli" uniqKey="Wu H" first="Hongli" last="Wu">Hongli Wu</name>
<name sortKey="Wu, Hongli" sort="Wu, Hongli" uniqKey="Wu H" first="Hongli" last="Wu">Hongli Wu</name>
<name sortKey="Xavier, Christy" sort="Xavier, Christy" uniqKey="Xavier C" first="Christy" last="Xavier">Christy Xavier</name>
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